Specific Genes Increase the Risk of Bedwetting (Biology)

In a large-scale study of Danish children and young people, researchers from Aarhus University have for the first time found genetic variants that increase the risk of nocturnal enuresis – commonly known as bedwetting or nighttime incontinence. The findings provide completely new insights into the processes in the body causing this widespread phenomenon.

Researchers have long known that nighttime incontinence is a highly heritable condition. Children who wet the bed at night often have siblings or parents who either suffer from or have suffered from the same condition. But until now, science has been unable to pinpoint the genes concerned.

In collaboration with the Danish research project iPSYCH and a team of international colleagues, researchers from Aarhus University have for the first time identified genetic variants that increase the risk of bedwetting. The results have just been published in the scientific journal The Lancet Child & Adolescent Health.

“As many as sixteen per cent of all seven-year-olds suffer from nocturnal enuresis and although many of them grow out of it, one to two per cent of all young adults still have this problem. It is a serious condition, which can negatively affect children’s self-esteem and well-being. For example, the children may be afraid of being bullied, and often opt out of events that involve overnight stays,” says Jane Hvarregaard Christensen, who is one of the researchers behind the study.

Regulates urine production

In the study, the researchers studied the genes of 3,900 Danish children and young people, who had either been diagnosed with nocturnal enuresis or had taken medication for it. This group was subsequently compared to 31,000 children and young people who did not suffer from the problem.

“We identified two locations in the genome where specific genetic variants increase the risk of bedwetting. The potential causal genes which we point to play roles in relation to ensuring that our brain develops the ability to keep urine production down at night, that the bladder’s activity is regulated and registered, and that we sleep in an appropriate way, among other things,” explains first author of the study, Cecilie Siggaard Jørgensen.

The study also shows that commonly occurring genetic variants can explain up to one-third of the genetic risk of bedwetting. This means that genetic variants which all of us have may lead to involuntary nocturnal enuresis, when they occur in a certain combination.

“But you can still also have all the variants without wetting the bed at night, because there are other risk factors in play that we haven’t mapped yet – both genetic and environmental. So it’s clear that this is very complex and that it’s not possible to talk about a single gene that causes nocturnal enuresis,” says Jane Hvarregaard Christensen.

Particularly vulnerable

The study also shows that children with many genetic variants that increase the risk of ADHD are particularly vulnerable to developing bedwetting.

“Our findings don’t mean that ADHD causes bedwetting in a child, or vice versa, but just that the two conditions have common genetic causes. More research in this area will be able to clarify the details in the biological differences and similarities between the two disorders,” she emphasises.

As the study is a first-time study, the researchers also examined more than 5,500 people from Iceland, where they found that the same genetic variants also appear to increase the risk of nocturnal enuresis.

“This means that we can be more certain that our findings are not coincidental. In the future, we wish to find out whether the same genetic variants increase the risk of bedwetting in children in other parts of the world. Bedwetting is not just an issue in northern European but affects millions of children all over the world,” she says.

The researchers hope to be able to further clarify the causes of nocturnal enuresis. It is very likely that it will be possible to identify even more genes and thereby gain a deeper understanding of what is required for a child to become dry at night.

“At present we still can’t use a child’s genetic profile to predict, for example, whether the child will grow out of its condition or whether a particular treatment works. Perhaps this will be possible in the future when more detailed studies have been conducted,” says Jane Hvarregaard Christensen.

Behind the results

The study is a so-called genome-wide association study (GWAS). By examining thousands of genetic variants spread out in the entire genome, a GWAS makes it possible to point to statistically significant correlations between specific genetic variants and nighttime incontinence in the persons who are examined.

The study is a collaboration between researchers at the Department of Biomedicine, Aarhus University and the Department of Paediatrics and Adolescent Medicine, Aarhus University Hospital. Researchers from the Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, and deCODE genetics have also contributed.

The study is financed by the Lundbeck Foundation and the Stanley Foundation.

Reference: Cecilie S Jørgensen, Veera M Rajagopal, Jakob Grove et al., “Identification of genetic loci associated with nocturnal enuresis: a genome-wide association study”, The Lancet, 2021. https://doi.org/10.1016/S2352-4642(20)30350-3 https://www.thelancet.com/journals/lanchi/article/PIIS2352-4642(20)30350-3/fulltext

Provided by Aarhus University

Aphids Suck: Invasive Aphid Found on Danish Apple Trees (Biology)

The spirea aphid, Aphis spiraecola, an invasive pest, has been discovered for the first time in Denmark by University of Copenhagen researchers. The extent of its current distribution remains unknown, but in time, it could prove to be a troublesome pest for Danish apple growers.

Whether the discovery of this aphid in Denmark is an isolated incident, or if the species has made itself at home due to a milder climate, remains unknown to the researchers. Closer investigation is needed. Photo: UCPH/Uni.Budapest

In a collaboration with colleagues at the University of Budapest, University of Copenhagen researchers have analysed and compared a number of samples of green aphids from apples around the world and discovered a new apple-loving pest in Denmark.

The bright greenish yellow spirea aphid—Aphis spiraecola— which most likely originates in East Asia, has gradually become a widespread pest in tropical and temperate regions around the planet. While it is especially problematic for citrus and apple trees, it can attack many other plant species. The aphid has been in the United States for the last 100 years and was discovered in Mediterranean countries in 1939. However, the spirea aphid has never been witnessed in the Nordic countries before.

“It is a serious pest that is more well known in countries a touch warmer than Denmark and is particularly harmful to citrus crops. It was identified in Germany in 2000, and the Baltic states a few years later. Now, it is here in Denmark. So, this is definitely something that we need to keep an eye on, as it could prove to be problematic for Danish apple growers,” warns Associate Professor Lene Sigsgaard of the University of Copenhagen’s Department of Plant and Environmental Sciences. For the past 20 years, Sigsgaard has researched natural predators and pest regulation in apple and other species.

Sucks nourishment out of the plants upon which it poos

Aphids have specialised mouth parts designed to pierce and suck nourishment from plants. Their liquid excrement, honeydew, is characterized by sticky areas on leaves and fruit. Sooty mold spores are captured by and can grow in the sticky honeydew coating a leaf, causing affected leaves to become dark, which blocks sunlight and reduces photosynthesis.

“Aphids can affect a plant in several ways. Among other things, they suck nourishment from plants, energy that would have otherwise been used to produce new shoots and fruits. This stresses plants and can reduce yields in both the current and following season,” explains Lene Sigsgaard. 

While the rosy apple aphid is currently enemy number one in Danish apple orchards, the bright green spiraea aphid could cause problems too. Only the future can tell what this little sucker’s ultimate impact will be.  

Virus spreaders

Aphis spiraecola is a virus vector on citrus fruit and can also spread plum pox virus, also called Sharka, which has yet to be observed in Denmark.

Whether the discovery of this aphid in Denmark is an isolated incident, or if the species has made itself at home due to a milder climate, remains unknown to the researchers. Closer investigation is needed.

Its natural predators, which typically keep aphid populations in check and limit damage, could help to regulate this invasive new aphid.

With increased biodiversity in and around orchards and fields, readily catalyzed by planting flowering hedges and flower rows, populations of natural predators such as ladybirds, green lacewings, spiders, kissing bugs and parasitoid wasps can be supported to combat and reduce aphid populations.

Fact Box

Species: Aphis spiraecola Patch, also known as the spirea aphid or green citrus aphid (Hemiptera, Aphididae)
Physical appearance: Bright greenish yellow to apple green aphid easily confused with the green apple aphid (Aphis pomi), yet with minor morphological differences. The aphid often occurs in mixed colonies of other aphids.
Origin: Probably East Asia
Distribution: Now widespread over tropical and temperate regions worldwide. Can be spread with plant material. Winged generations during spring and late summer allow the species to spread themselves.
Host plants: Spirea, citrus, and apples are primary hosts where eggs are laid. The species also attacks other seed fruits, stone fruits, etc., and in the tropics, species including cocoa. The aphid can live on at least 20 different plant genera, making it very polyphagous.
Life: Across most of its range, the species reproduces asexually year-round (females give birth to new females without mating). In Denmark, the vast majority of aphid species winter as eggs, except for the peach aphid. Whether this new species will winter in Denmark as eggs or aphids in large numbers is unknown.
Impact: Commonly attacks citrus and apple trees. Aphids suck nourishment from plants. Sooty mold growing in honeydew can decrease a plant’s ability to photosynthesize. The aphid causes apple leaves to curl and may cause the tips of branches to produce abnormally little growth. Severely-infested leaves become small, bright and may fall prematurely. Symptoms are similar to those caused by green apple aphids.
Viruses: The species is a virus vector for several species including CTV on citrus and plum pox virus.

Read the research article: https://static-curis.ku.dk/portal/files/253648977/108_2020_PPS.pdf

Provided by University of Copenhagen

NAD+ Can Restore Age-related Muscle Deterioration (Biology)

The older we grow, the weaker our muscles get, riddling old age with frailty and physical disability. But this doesn’t only affect the individual, it also creates a significant burden on public healthcare. And yet, research efforts into the biological processes and biomarkers that define muscle aging have not yet defined the underlying causes.

Graphical abstract by Romani et al.

Now, a team of scientists from lab of Johan Auwerx at EPFL’s School of Life Sciences looked at the issue through a different angle: the similarities between muscle aging and degenerative muscle diseases. They have discovered protein aggregates that deposit in skeletal muscles during natural aging, and that blocking this can prevent the detrimental features of muscle aging. The study is published in Cell Reports.

“During age-associated muscle diseases, such as inclusion body myositis (IBM), our cells struggle to maintain correct protein folding, leading these misfolded proteins to precipitate and forming toxic protein aggregates within the muscles,” explains Auwerx. “The most prominent component of these protein aggregates is beta-amyloid, just like in the amyloid plaques in the brains of patients with Alzheimer’s disease.”

In the study, the scientists identify amyloid-like protein aggregates in aged muscles from different species, from the nematode C. elegans all the way to humans. In addition, they also found that these aggregates also impair mitochondrial function. Although aggregated proteins have been suggested to contribute to brain aging, this is the first time that they have been shown to contribute to muscle aging and to directly damage mitochondria. “These abnormal proteotoxic aggregates could serve as novel biomarkers for the aging process, beyond the brain and muscle,” says Auwerx.

But can the formation of the protein aggregates be reversed? To answer this, the researchers fed worms the vitamin nicotinamide riboside and the antitumor agent Olaparib, both of which boost the levels of nicotinamide adenine dinucleotide (NAD+), a biomolecule that is essential for maintaining mitochondrial function, and whose levels decline during aging.

In the worms, the two compounds turned on the defense systems of the mitochondria, even when provided at advanced age. Turning on the so-called “mitochondrial quality control system” reduced the age-related amyloid protein aggregates and improved the worms’ fitness and lifespan.

The scientists then moved on to human muscle tissue, taken from aged subjects and IBM patients. Turning on the same mitochondrial quality control systems produced similar improvements in protein and mitochondrial homeostasis. The encouraging results led the researchers to test nicotinamide riboside in aged mice. The treatment also activated the mitochondrial defense systems and reduced the number and size of amyloid aggregates in different skeletal muscle tissues.

“Drugs that boost mitochondrial quality control could therefore be tested in the clinic to reverse these age-related proteotoxic aggregates and rejuvenate tissues,” says Mario Romani, the first author of the study.

Reference: Mario Romani, Vincenzo Sorrentino, Chang-Myung Oh, Hao Li, Tanes Imamura de Lima, Hongbo Zhang, Minho Shong, Johan Auwerx. NAD+ boosting reduces age-associated amyloidosis and restores mitochondrial homeostasis in muscle. Cell Reports 19 January 2021. https://www.cell.com/cell-reports/fulltext/S2211-1247(20)31649-1?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124720316491%3Fshowall%3Dtrue DOI: 10.1016/j.celrep.2020.108660

Provided by EPFL

Snap-freezing Reveals a Truer Structure of Brain Connections (Neuroscience)

Scientists at EPFL have used a snap-freezing method to reveal the true structure of the connections that join neurons together in the adult brain.

Most synaptic connections in the adult brain are situated on dendritic spines; small, micrometer-long, protrusions extending from the neurons’ surface. The spines’ exact size and shape determine how well signals are passed from one neuron to another.

3D model of dendritic spines (purple) making synapses with axons containing vesicles (yellow). Background shows electron microscope image of brain tissue. Credit: Graham Knott (EPFL)

These details become very important when neuroscientists want to model brain circuits or understand how information is transmitted between neurons across the brain’s neuronal circuits. However, their small size and the difficulties in preserving brain tissue in its natural state have always left the question open as to what the true structure of the dendritic spine is.

Scientists from EPFL’s School of Life Sciences have now used a snap-freezing method of liquid nitrogen jets, combined with very high pressures, to instantaneously preserve small pieces of brain tissue. The researchers, from the labs of Graham Knott and Carl Petersen, then used high-resolution, 3D imaging with electron microscopes to reveal how the true dendritic spine structure was similar to that shown in previous studies, except for one important aspect: The instant freezing method showed dendritic spines with significantly thinner necks.

This finding validates a considerable body of theoretical and functional data going back many years, which shows that dendritic spines are chemical, as well as electrical, compartments isolated from the rest of the neuron by a thin and high-resistance neck. Variations in the neck diameter have an important impact on how a synapse influences the rest of the neuron.

“As well as revealing the true shape of these important brain structures, this work highlights the usefulness of rapid freezing methods and electron microscopy for obtaining a more detailed view of the architecture of cells and tissues,” says Graham Knott.

Funding: (1) Young Researchers Exchange Programme between Japan and Switzerland (Japanese-Swiss Science and Technology Programme) (2) JSPS KAKENHI grant (3) Swiss National Science Foundation

References: Tamada H, Blanc J, Korogod N, Petersen CCH, Knott GW. Ultrastructural comparison of dendritic spine morphology preserved with cryo and chemical fixation. eLife 2020;9:e56384. https://elifesciences.org/articles/56384 DOI: 10.7554/eLife.56384

Provided by EPFL

Gene-Editing ‘Scissor’ Tool May Also be a ‘Dimmer Switch’ (Medicine)

CRISPR technology shown to ‘dial down’ gene activity in bacteria.

In a series of experiments with laboratory-cultured bacteria, Johns Hopkins scientists have found evidence that there is a second role for the widely used gene-cutting system CRISPR-Cas9 — as a genetic dimmer switch for CRISPR-Cas9 genes. Its role of dialing down or dimming CRISPR-Cas9 activity may help scientists develop new ways to genetically engineer cells for research purposes.

A summary of the findings was published Jan. 8 in Cell.

Left – a schematic of the long form of the tracrRNA used by the CRISPR-Cas9 system in bacteria; Right – the standard guide RNA used by many scientists as part of the gene-cutting CRISPR-Cas9 system. Credit: Joshua Modell, Rachael Workman and Johns Hopkins Medicine

First identified in the genome of gut bacteria in 1987, CRISPR-Cas9 is a naturally occurring but unusual group of genes with a potential for cutting DNA sequences in other types of cells that was realized 25 years later. Its value in genetic engineering — programmable gene alteration in living cells, including human cells — was rapidly appreciated, and its widespread use as a genome “editor” in thousands of laboratories worldwide was recognized in the awarding of the Nobel Prize in Chemistry last year to its American and French co-developers.

CRISPR stands for clustered, regularly interspaced short palindromic repeats. Cas9, which refers to CRISPR-associated protein 9, is the name of the enzyme that makes the DNA slice. Bacteria naturally use CRISPR-Cas9 to cut viral or other potentially harmful DNA and disable the threat, says Joshua Modell, Ph.D., assistant professor of molecular biology and genetics at the Johns Hopkins University School of Medicine. In this role, Modell says, “CRISPR is not only an immune system, it’s an adaptive immune system — one that can remember threats it has previously encountered by holding onto a short piece of their DNA, which is akin to a mug shot.” These mug shots are then copied into “guide RNAs” that tell Cas9 what to cut.

Scientists have long worked to unravel the precise steps of CRISPR-Cas9’s mechanism and how its activity in bacteria is dialed up or down. Looking for genes that ignite or inhibit the CRISPR-Cas9 gene-cutting system for the common, strep-throat causing bacterium Streptococcus pyogenes, the Johns Hopkins scientists found a clue regarding how that aspect of the system works.

Specifically, the scientists found a gene in the CRISPR-Cas9 system that, when deactivated, led to a dramatic increase in the activity of the system in bacteria. The product of this gene appeared to re-program Cas9 to act as a brake, rather than as a “scissor,” to dial down the CRISPR system.

“From an immunity perspective, bacteria need to ramp up CRISPR-Cas9 activity to identify and rid the cell of threats, but they also need to dial it down to avoid autoimmunity — when the immune system mistakenly attacks components of the bacteria themselves,” says graduate student Rachael Workman, a bacteriologist working in Modell’s laboratory.

To further nail down the particulars of the “brake,” the team’s next step was to better understand the product of the deactivated gene (tracrRNA). RNA is a genetic cousin to DNA and is vital to carrying out DNA “instructions” for making proteins. TracrRNAs belong to a unique family of RNAs that do not make proteins. Instead, they act as a kind of scaffold that allows the Cas9 enzyme to carry the guide RNA that contains the mug shot and cut matching DNA sequences in invading viruses.

TracrRNA comes in two sizes: long and short. Most of the modern gene-cutting CRISPR-Cas9 tools use the short form. However, the research team found that the deactivated gene product was the long form of tracrRNA, the function of which has been entirely unknown.

The long and short forms of tracrRNA are similar in structure and have in common the ability to bind to Cas9. The short form tracrRNA also binds to the guide RNA. However, the long form tracrRNA doesn’t need to bind to the guide RNA, because it contains a segment that mimics the guide RNA. “Essentially, long form tracrRNAs have combined the function of the short form tracrRNA and guide RNA,” says Modell.

In addition, the researchers found that while guide RNAs normally seek out viral DNA sequences, long form tracrRNAs target the CRISPR-Cas9 system itself. The long form tracrRNA tends to sit on DNA, rather than cut it. When this happens in a particular area of a gene, it prevents that gene from expressing, — or becoming functional.

To confirm this, the researchers used genetic engineering to alter the length of a certain region in long form tracrRNA to make the tracrRNA appear more like a guide RNA. They found that with the altered long form tracrRNA, Cas9 once again behaved more like a scissor.

Other experiments showed that in lab-grown bacteria with a plentiful amount of long form tracrRNA, levels of all CRISPR-related genes were very low. When the long form tracrRNA was removed from bacteria, however, expression of CRISPR-Cas9 genes increased a hundredfold.

Bacterial cells lacking the long form tracrRNA were cultured in the laboratory for three days and compared with similarly cultured cells containing the long form tracrRNA. By the end of the experiment, bacteria without the long form tracrRNA had completely died off, suggesting that long form tracrRNA normally protects cells from the sickness and death that happen when CRISPR-Cas9 activity is very high.

“We started to get the idea that the long form was repressing but not eliminating its own CRISPR-related activity,” says Workman.

To see if the long form tracrRNA could be re-programmed to repress other bacterial genes, the research team altered the long form tracrRNA’s spacer region to let it sit on a gene that produces green fluorescence. Bacteria with this mutated version of long form tracrRNA glowed less green than bacteria containing the normal long form tracrRNA, suggesting that the long form tracrRNA can be genetically engineered to dial down other bacterial genes.

Another research team, from Emory University, found that in the parasitic bacteria Francisella novicida, Cas9 behaves as a dimmer switch for a gene outside the CRISPR-Cas9 region. The CRISPR-Cas9 system in the Johns Hopkins study is more widely used by scientists as a gene-cutting tool, and the Johns Hopkins team’s findings provide evidence that the dimmer action controls the CRISPR-Cas9 system in addition to other genes.

The researchers also found the genetic components of long form tracrRNA in about 40% of the Streptococcus group of bacteria. Further study of bacterial strains that don’t have the long form tracrRNA, says Workman, will potentially reveal whether their CRISPR-Cas9 systems are intact, and other ways that bacteria may dial back the CRISPR-Cas9 system.

The dimmer capability that the experiments uncovered, says Modell, offers opportunities to design new or better CRISPR-Cas9 tools aimed at regulating gene activity for research purposes. “In a gene editing scenario, a researcher may want to cut a specific gene, in addition to using the long form tracrRNA to inhibit gene activity,” he says.

Funding for the Johns Hopkins research was provided by the Johns Hopkins University School of Medicine.

Other scientists who contributed to the research include Teja Pammi, Binh Nguyen, Leonardo Graeff, Erika Smith, Suzanne Sebald and Marie Stoltzfus from Johns Hopkins, and Chad Euler from Weill Cornell Medical College.

Reference: Rachael Workman, Teja Pammi et al., “A natural single-guide RNA repurposes Cas9 to autoregulate CRISPR-Cas expression”, Cell, 2021. https://doi.org/10.1016/j.cell.2020.12.017

Provided by Johns Hopkins Medicine

New Insights into Wound Healing Process (Biology)

For the first time, scientists watch fibroblasts, key cell type involved in wound healing, coordinate closure of damaged vascularized tissue.

Biomedical engineers developed a technique to observe wound healing in real time, discovering a central role for cells known as fibroblasts. The work, reported in APL Bioengineering, by AIP Publishing, is the first demonstration of a wound closure model within human vascularized tissue in a petri dish.

Biomedical engineers have developed a technique to observe wound healing in real time, discovering a central role for cells known as fibroblasts. The work is the first demonstration of a wound closure model within human vascularized tissue in a petri dish. This image shows steps in wound healing in a model system. © Jeroen Eyckmans, Juliann B. Tefft

Prior investigations of wound healing have used animal models, but healing in humans does not occur the same way. One difference is that wounds in mice and rats, for example, can heal without granulation tissue, a type of tissue critical to the healing of human wounds.

Granulation tissue forms after blood coagulates, and the wound scabs over. Coagulation creates a fibrin network that serves as a temporary matrix. Granulation tissue then takes over, filling the wound with new tissue and blood capillaries, protecting the wound from infection, and providing a foundation for further healing.

The investigators created a wound model by mixing human cells into a gel composed of fibrin and collagen. Blood vessels formed in the gel, producing what is known as vascularized tissue. Two cell types were used: human endothelial cells and fibroblasts, both of which are present in a natural wound.

Fibroblasts are natural fiber-producing cells found in most organs and connective tissue. Endothelial cells form the lining of blood vessels and regulate exchange between the bloodstream and other tissues. When a wound heals, new blood vessels form in a process known as angiogenesis.

Within three days, the mix of cells in the experimental gel had formed a network of capillaries. At this point, the tissues were cut with a diamond dissection knife, producing a wound through the full thickness of the tissue. It took four days for the wound to fully close, but cells were observed migrating into the wound by day 3.

“The migration of the fibroblasts and endothelial cells were tracked over the course of 90 hours, revealing rapid movement of fibroblasts around the wound edge and slower motion by endothelial cells,” said author Juliann Tefft.

The investigators observed fibroblasts circling the edge of the wound for about 50 hours, when the cells began to close the void. A series of subsequent experiments using varying amounts of fibroblasts and endothelial cells revealed that tissues with endothelial cells alone had not healed even after 10 days.

“This evidence supports the hypothesis that fibroblasts are the primary drivers of wound closure,” said author Jeroen Eyckmans. “In our system, the endothelial cells, needed for angiogenesis, the formation of new capillaries, didn’t repopulate the healed tissue that was filled in by the fibroblasts. For this reason, our model could be a useful bottom-up system to investigate the minimum components required for appropriate wound angiogenesis.”

The article “Reconstituting the dynamics of endothelial cells and fibroblasts in wound closure” is authored by Juliann B. Tefft, Christopher S. Chen, and Jeroen Eyckmans. The article will appear in APL Bioengineering on Jan. 19, 2021 (DOI: 10.1063/5.0028651). After that date, it can be accessed at https://aip.scitation.org/doi/10.1063/5.0028651.

Provided by American Institute of Physics

50 Million-year-old Fossil Assassin Bug Has Unusually Well-preserved Genitalia (Archeology)

The fossilized insect is tiny and its genital capsule, called a pygophore, is roughly the length of a grain of rice. It is remarkable, scientists say, because the bug’s physical characteristics – from the bold banding pattern on its legs to the internal features of its genitalia – are clearly visible and well-preserved. Recovered from the Green River Formation in present-day Colorado, the fossil represents a new genus and species of predatory insects known as assassin bugs.

Recovered from the Green River Formation in present-day Colorado, this fossil represents a new genus and species of predatory insects known as assassin bugs. Researchers named the specimen Aphelicophontes danjuddi. A small beetle was also fossilized with the specimen. Photos by Daniel Swanson /Courtesy Palaeontological Association

The find is reported in the journal Papers in Palaeontology.

Discovered in 2006 by breaking open a slab of rock, the fossilized bug split almost perfectly from head to abdomen. The fracture also cracked the pygophore in two. A fossil dealer later sold each half to a different collector, and the researchers tracked them down and reunited them for this study.

Being able to see a bug’s genitalia is very helpful when trying to determine a fossil insect’s place in its family tree, said Sam Heads, a paleontologist at the Illinois Natural History Survey and self-described fossil insect-genitalia expert who led the research with Daniel Swanson, a graduate student in entomology at the University of Illinois Urbana-Champaign.

Species are often defined by their ability to successfully mate with one another, and small differences in genitalia can lead to sexual incompatibilities that, over time, may result in the rise of new species, Swanson said. This makes the genitalia a good place to focus to determine an insect species.

But such structures are often obscured in compression fossils like those from the Green River Formation.

U. of I. entomology graduate student Daniel Swanson co-led the research on an ancient assassin bug fossil. Photo by L. Brian Stauffer

“To see these fine structures in the internal genitalia is a rare treat,” Swanson said. “Normally, we only get this level of detail in species that are living today.”

The structures visible within the pygophore include the basal plate, a hardened, stirrup-shaped structure that supports the phallus, he said. The fossil also preserved the contours of the phallotheca, a pouch into which the phallus can be withdrawn.

The find suggests that the banded assassin bugs, a group to which the new specimen is thought to belong, are about 25 million years older than previously thought, Swanson said.

“There are about 7,000 species of assassin bug described, but only about 50 fossils of these bugs are known,” he said. “This just speaks to the improbability of even having a fossil, let alone one of this age, that offers this much information.”

This is not the oldest fossil bug genitalia ever discovered, however.

Illinois Natural History Survey paleontologist Sam Heads co-led the study of an extraordinarily well-preserved 50 million-year-old fossil insect. Photo by L. Brian Stauffer

“The oldest known arthropod genitalia are from a type of bug known as a harvestman that is 400-412 million years old, from the Rhynie Chert of Scotland,” Heads said. “And there are also numerous fossil insects in amber as old as the Cretaceous Period with genitalia preserved.

“However, it is almost unheard of for internal male genitalia to be preserved in carbonaceous compressions like ours,” he said.

The researchers named the new assassin bug Aphelicophontes danjuddi. The species name comes from one of the fossil collectors, Dan Judd, who donated his half of the specimen to the INHS for study.

The INHS is a division of the Prairie Research Institute at the U. of I.

The National Science Foundation supported this work.

The paper “A new remarkably preserved fossil assassin bug (Insecta, Heteroptera, Reduviidae) from the Eocene Green River Formation of Colorado” is available from the U. of I. News Bureau. DOI: 10.1002/spp2.1349

Provided by University of Illinois

All-purpose Dinosaur Opening Reconstructed for the First Time (Paleontology)

For the first time ever, a team of scientists, led by the University of Bristol, have described in detail a dinosaur’s cloacal or vent – the all-purpose opening used for defecation, urination and breeding.

A reconstruction of Psittacosaurus illustrating how the cloacal vent may have been used for signalling during courtship. © Bob Nicholls/Paleocreations.com 2020

Although most mammals may have different openings for these functions, most vertebrate animals possess a cloaca. 

Although we know now much about dinosaurs and their appearance as feathered, scaly and horned creatures and even which colours they sported, we have not known anything about how the vent appears.

Dr Jakob Vinther from the University of Bristol’s School of Earth Sciences, along with colleagues Robert Nicholls, a palaeoartist, and Dr Diane Kelly, an expert on vertebrate penises and copulatory systems from the University of Massachusetts Amherst, have now described the first cloacal vent region from a small Labrador-sized dinosaur called Psittacosaurus, comparing it to vents across modern vertebrate animals living on land.

Dr Vinther said: “I noticed the cloaca several years ago after we had reconstructed the colour patterns of this dinosaur using a remarkable fossil on display at the Senckenberg Museum in Germany which clearly preserves its skin and colour patterns.

Close up of the preserved cloacal vent in Psittacosaurus and the authors’ reconstruction of it. © Kelly et al.

“It took a long while before we got around to finish it off because no one has ever cared about comparing the exterior of cloacal openings of living animals, so it was largely unchartered territory.”

Dr Kelly added: “Indeed, they are pretty non-descript. We found the vent does look different in many different groups of tetrapods, but in most cases it doesn’t tell you much about an animal’s sex.

“Those distinguishing features are tucked inside the cloaca, and unfortunately, they’re not preserved in this fossil.”

The cloaca is unique in its appearance but exhibits features reminiscent to living crocodylians such as alligators and crocodiles, which are the closest living relatives to dinosaurs and other birds.

The researchers note that the outer margins of the cloaca are highly pigmented with melanin. They argue that this pigmentation provided the vent with a function in display and signalling, similar to living baboons and some breeding salamanders.

Psittacosaurus specimen from Senckenberg museum of Natural History, preserving skin and pigmentation patterns and the first, and only known, cloacal vent. © Jakob Vinther, University of Bristol and Bob Nicholls/Paleocreations.com 2020

The authors also speculate that the large, pigmented lobes on either side of the opening could have harboured musky scent glands, as seen in living crocodylians.

Birds are one the few vertebrate groups that occasionally exhibit visual signalling with the cloaca, which the scientists now can extend back to the Mesozoic dinosaur ancestors.

Robert Nicholls said: “As a palaeoartist, it has been absolutely amazing to have an opportunity to reconstruct one of the last remaining features we didn’t know anything about in dinosaurs.

“Knowing that at least some dinosaurs were signalling to each other gives palaeoartists exciting freedom to speculate on a whole variety of now plausible interactions during dinosaur courtship. It is a game changer!”

Reference: ‘A cloacal opening in a non-avian dinosaur’ by J. Vinther, R. Nicholls and D. Kelly in Current Biology, 2021. https://www.cell.com/current-biology/fulltext/S0960-9822(20)31891-1?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0960982220318911%3Fshowall%3Dtrue

Provided by University of Bristol

Study Shows Tweaking One Layer of Atoms on a Catalyst’s Surface Can Make it Work Better (Material Science)

The surprising results offer a way to boost the activity and stability of catalysts for making hydrogen fuel from water.

Scientists crafting a nickel-based catalyst used in making hydrogen fuel built it one atomic layer at a time to gain full control over its chemical properties. But the finished material didn’t behave as they expected: As one version of the catalyst went about its work, the top-most layer of atoms rearranged to form a new pattern, as if the square tiles that cover a floor had suddenly changed to hexagons.

But that’s ok, they reported today, because understanding and controlling this surprising transformation gives them a new way to turn catalytic activity on and off and make good catalysts even better.

The research team, led by scientists from Stanford University and the Department of Energy’s SLAC National Accelerator Laboratory, described their study in Nature Materials today.

“Catalysts can change very quickly during the course of a reaction, and understanding how they transform from an inactive phase to an active one is crucial to designing more efficient catalysts,” said Will Chueh, an investigator with the Stanford Institute for Materials and Energy Sciences (SIMES) at SLAC who led the study. “This transformation gives us the equivalent of a knob we can turn to fine-tune their behavior.”

An illustration combines two possible types of surface layers for a catalyst that performs the water-splitting reaction, the first step in making hydrogen fuel. The gray surface, top, is lanthanum oxide. The colorful surface is nickel oxide; a rearrangement of its atoms while carrying out the reaction made it twice as efficient, a phenomenon researchers hope to harness to design better catalysts. Lanthanum atoms are depicted in green, nickel in blue and oxygen in red. (CUBE3D Graphic)

Splitting water to make hydrogen fuel

Catalysts help molecules react without being consumed in the reaction, so they can be used over and over. They’re the backbone of many green-energy devices.

This particular catalyst, lanthanum nickel oxide or LNO, is used to split water into hydrogen and oxygen in a reaction powered by electricity. It’s the first step in generating hydrogen fuel, which has enormous potential for storing renewable energy from sunlight and other sources in a liquid form that’s energy-rich and easy to transport. In fact, several manufacturers have already produced electric cars powered by hydrogen fuel cells.

But this first step is also the most difficult one, said Michal Bajdich, a theorist at the SUNCAT Center for Interface Science and Catalysis at SLAC, and researchers have been searching for inexpensive materials that will carry it out more efficiently.

Since reactions take place on a catalyst’s surface, researchers have been trying to precisely engineer those surfaces so they promote only one specific chemical reaction with high efficiency.

Building materials one atomic layer at a time

The LNO investigated in this study belongs to a class of promising catalytic materials known as perovskites, named after a natural mineral with a similar atomic structure.

Christoph Baeumer, who came to SLAC as a Marie Curie Fellow from Aachen University in Germany to carry out the study, prepared LNO in what’s known as an epitaxial thin film – a film grown in atomically thin layers in a way that creates an extraordinarily precise arrangement of atoms.

Dividing his time between California and Germany, Baeumer made two versions of the film at different temperatures ­­– one with a nickel-rich surface and another with a lanthanum-rich surface. Then the research team ran all the versions through the water-splitting reaction to compare how well they performed.

“We were surprised to discover that the films with nickel-rich surfaces carried out the reaction twice as fast,” Baeumer said.

A new study shows how tweaking the surface layer of a catalyst can make it work better. This particular catalyst is used to split water, the first step in making hydrogen fuel. It consists of alternating layers of materials rich in nickel (blue spheres) and lanthanum (green spheres; the red spheres represent oxygen atoms). When the material is grown at relatively cool temperatures so a nickel-rich layer is on top (left), the atoms on that surface layer rearrange during the water-splitting reaction (middle) in a way that allows them to carry out the reaction more efficiently (right). This surprising result gives scientists a new way to tune catalytic activity and engineer better catalysts. (Tomas Duchon/Forschungszentrum Juelich)

Tuning a catalyst’s surface for better performance

To find out why, the team took the films to DOE’s Lawrence Berkeley National Laboratory, where a group led by Slavomír Nemšák looked at their atomic structure with X-rays at the Advanced Light Source.

“It was surprising that the difference between the ‘good’ and the ‘bad’ catalyst was only in the last atomic layer of the films,” Nemšák said. Those investigations also revealed that in films with nickel-rich surface layers that were prepared at cooler temperatures, the top layer of atoms transformed at some point during the water-splitting reaction, and this new arrangement boosted the catalytic activity.

Meanwhile, Jiang Li, a postdoctoral researcher and theorist at SUNCAT, performed computational studies of this very complex system using Berkeley Lab’s National Energy Research Scientific Computing Center (NERSC). His conclusions agreed with the experimental results, predicting that the version of the catalyst with the transformed surface – from a cubic pattern to a hexagonal one – would be the most active and stable one.

Bajdich said, “Is the transformation of the nickel-rich surface driven by the way the catalyst is prepared, or by changes it undergoes while it carries out the water-splitting reaction? That’s very hard to answer. It looks like both have to occur.”

Although this particular catalyst is not the best in the world for splitting water into hydrogen and oxygen, he said, discovering how a surface transformation boosts its activity is important and could potentially apply to other materials too.

“If we can unlock the secrets of this transformation so we can accurately tune it,” he said, “then we can leverage this phenomenon to make much better catalysts in the future.”

The Advanced Light Source and the National Energy Research Scientific Computing Center are DOE Office of Science user facilities. Scientists from Forschungszentrum Juelich in Germany also contributed to this research. The project was funded by the DOE Office of Science, and Baeumer was also supported by the European Union’s Horizon 2020 research and innovation program through a Marie Sklodowska-Curie fellowship.

Reference: Baeumer, C., Li, J., Lu, Q. et al. Tuning electrochemically driven surface transformation in atomically flat LaNiO3 thin films for enhanced water electrolysis. Nat. Mater. (2021). https://doi.org/10.1038/s41563-020-00877-1 (10.1038/s41563-020-00877-1)

Provided by SLAC